최신연구결과(해외)

NeoplasmIncomplete Intestinal Metaplasia is Rare in Autoimmune Gastritis

관리자
2023-04-21
조회수 1131

2023년 2월 Digestive disease에 실린 내용입니다. 2023년이 시작하면서 AIG의 화두 중 하나는 <과연, AIG는 gastric cancer risk가 있는 질환인가> 입니다. 

* Autoimmune gastritis: long-term natural history in naïve Helicobacter pylori-negative patients. Rugge M, Bricca L, Guzzinati S, Sacchi D, et al. Gut. 2023 Jan;72(1):30-38.

* No H. pylori, no adenocarcinoma for patients with autoimmune gastritis. Goldenring J.Gut. 2023 Jan;72(1):1-2.


Helicobacter pylori (Hp) 감염되지 않은 AIG에서 gastric cancer (GC)가 발생하는지에 대한 물음을 던지는 논문이 나왔고, 이에 대하여 gastric cancer risk가 있다는 의견들이 letter 형식으로 실렸고 AIG환자에서의 neoplasia에 대한 meta 분석도 나왔습니다. 

* Conclusion that autoimmune gastritis does not predispose to gastric cancer is unproven. Waldum HL.Gut. 2023 Jan 24:gutjnl-2022-329323.

* Unravelling the risk of developing gastric cancer in autoimmune gastritis. Lenti MV, Broglio G, Di Sabatino A. Gut. 2022 Aug 18:gutjnl-2022-328345. 

* Gastric cancer risk in autoimmune gastritis: evidence versus opinion. Rugge M, Genta RM, Malfertheiner P, Graham DY. Gut. 2023 Feb 27:gutjnl-2023-329618.

* Incidence of Gastric Neoplasms Arising from Autoimmune Metaplastic Atrophic Gastritis: A Systematic Review and Case Reports.

Chen C, Yang Y, Li P, Hu H.J Clin Med. 2023 Jan 30;12(3):1062. 

하지만, 여전히 관련 질문에 대해 여러 석학들의 의견이 분분한 시점에 이 논문이 나왔습니다. Intestinal metaplasia (IM) 는 complete type과 incomplete type으로 나누어지게 되고 incomplete type의 IM에서 malignancy와의 연관성이 높다고 알려져 있고, Hp gastritis와 AIG 사이의 imcomplete type IM의 빈도가 다르다는 내용입니다. 내용을 살펴 보도록 하겠습니다. 


Figure 1. We defined as grade 1 IM (G1-IM) the finding of an isolated metaplastic gland or small groups of metaplastic glands, stained with hematoxylin and eosin (H&E) in panel A and with Alcian Blue – Periodic Acid Schiff, or ABPAS, in panel B. This finding, which may result from the healing of minute gastric mucosal lesions, is usually characterized by a complete-type appearance of the IM and is most common in either normal or minimally inflamed stomachs. Original magnification 10x for both images


Figure 2. Panel A shows a hematoxylin and eosin (H&E) stained section of gastric mucosa with complete IM. The similarity with small intestinal mucosa is even more evident in panel B (stained with Alcian Blue – Periodic Acid Schiff, or ABPAS), where the orderly distribution of the goblet cells and the brush border are clearly discernible. Panel C shown the brush border stained as a continuous dark line with anti-CD 10 immunohistochemical stain. In contrast, panel D shows the incomplete type of gastric IM. Its colonic appearance (disorderly distribution of goblet cells of variable sizes, absence of brush border) is clearly visible in the ABPAS section (panel E). In panel F, a completely negative CD 10 staining confirms the absence of a brush border. Original magnification 10x for all images.


The percentage of patients with incomplete IM. Fifty-two of the 138 patients with H. pylori gastritis (37.7%) had incomplete IM. Amongst the 141 patients with IM arising in reactive gastropathy, 7 (5.0%) had incomplete IM. None of 59 patients with IM micro-foci in a gastric mucosa with no other pathological changes had incomplete IM. Atrophic autoimmune gastritis was associated with incomplete IM in 4 of the 48 patients included (8.3%).

Table 1. Demographics and prevalence of incomplete IM by diagnostic categories.

AIG = Auto-Immune Gastritis; IM = Intestinal Metaplasia; “Normal mucosa” indicates mucosa with small foci of IM in the absence of other pathological abnormalities. 


Amongst the 221 patients with grade 1 IM (G1-IM), 16 subjects had incomplete IM (7.3%) (Table 2). Of these, 12 occurred in H. pylori gastritis, 3 had reactive gastropathy, and one had AIG. Of the 165 patients with grade 2 IM (G2-IM), 47 (28.5%) had incomplete IM; 40 had H. pylori gastritis, 4 had reactive gastropathy, and 3 had AIG.

Table 2. Topographic distribution and extension of IM in different gastric phenotypes.

AIG = Auto-Immune Gastritis; IM = Intestinal Metaplasia; G1 and G2 = grade 1 and 2 Intestinal metaplasia; “Normal mucosa” indicates mucosa with small foci of IM in the absence of other pathological abnormalities. 


Patients with G2-IM were more than 6 times as likely to harbor incomplete metaplasia as those with G1-IM (OR = 6.69; 95% CI = 2.77 – 9.40).

Table 3. Correlation between IM grade and subtype.

IM = Intestinal Metaplasia; G1 and G2 = grade 1 and 2 Intestinal metaplasia; OR = odds ratio; CI = confidence interval 




ABSTRACT 

Background: Incomplete intestinal metaplasia (IM) is reportedly associated with higher gastric cancer (GC) risk than its complete variant. AGA Guidelines recommend including IM subtyping in routine pathology reports. This study assesses the prevalence of complete versus incomplete IM in gastric conditions with different GC risks. 

Methods: IM-subtyping (complete versus incomplete) and grading (IM extension: G1: ≤30%; G2: >30%) were assessed in 386 patients with IM+ve gastric biopsy sets that included both antral and oxyntic samples. Cases were categorized as: a) IM foci in otherwise normal mucosa (n = 59); b) H. pylori gastritis (n = 138); c) reactive gastropathy (141); d) Autoimmune atrophic gastritis (AIG, n = 48). Odds ratios (OR) and their 95%CI were used in comparing the prevalence of incomplete-IM and the correlation between subtype and IM extension. 

Results: Incomplete-IM was presents in 37.7% of patients with H. pylori gastritis; 8.3% of those with AIG; 5.0% of those with reactive gastropathy, and none of those with otherwise normal mucosa. Incomplete-IM was strongly associated with more extensive (G2-IM) mucosal intestinalization (OR=6.69; CI95%: 2.77 – 9.40). 

Conclusion: Incomplete-IM is significantly more prevalent in conditions (H. pylori gastritis) known to carry a higher risk of GC and is strongly associated with its extension. The low prevalence of incomplete IM in AIG (8.3%), and reactive gastropathy (5.2%) is in keeping with the low GC risk associated with these conditions.

0 0


대한자가면역성위염연구회

주소 : 경기도 용인시 기흥구 중부대로 579, 508-23호

대표전화 : 070-8080-0453

이메일 : autogastritis@gmail.com 


Copyright (c)대한자가면역성위염연구회. All Rights Reserved.

Design Hosting By 위멘토.


대한자가면역성위염연구회

주소 : 경기도 용인시 기흥구 중부대로 579, 508-23호 (구갈동, 강남대프라자)

대표전화 : 070-8080-0453  이메일 : autogastritis@gmail.com 


Copyright (c)대한자가면역성위염연구회. All Rights Reserved. Design Hosting By 위멘토.